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Tuesday, January 29, 2008

Hong Kong Flu

Compiled and Summarized by AnthonyHong Kong flu is a pandemic of influenza A (H3N2) in 1968-69. This virus was first detected in Hong Kong in early 1968 and spread to the United States later that year. where it caused about 34,000 deaths, making it the mildest pandemic in the 20th century. Also known as Hong Kong influenza.

There could be several reasons why fewer people in the US died due to this virus. First, the Hong Kong flu virus was similar in some ways to the Asian flu virus that circulated between 1957 and 1968. Earlier infections by the Asian flu virus might have provided some immunity against the Hong Kong flu virus that may have helped to reduce the severity of illness during the Hong Kong pandemic.

Second, instead of peaking in September or October, like pandemic influenza had in the previous two pandemics, this pandemic did not gain momentum until near the school holidays in December. Since children were at home and did not infect one another at school, the rate of influenza illness among schoolchildren and their families declined.

Third, improved medical care and antibiotics that are more effective for secondary bacterial infections were available for those who became ill.

Signs and Symptoms

The list of signs and symptoms mentioned in various sources for Flu includes the 20 symptoms listed below:

Note that Flu symptoms usually refers to various symptoms known to a patient, but the phrase Flu signs may refer to those signs only noticeable by a doctor.

Causative Agent

Influenza A (H3N2)

Mode of Transmission

H3N2 pandemic flu strains contained genes from avian influenza viruses. The new subtype arose in pigs co-infected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported re-assortment of divergent subtypes. However, other hosts appear capable of similar co-infection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible.

As an Influenza virus, it predominately transmitted by airborne spread in aerosols but can also be transferred by direct contact with droplets. Nasal inoculation after hand contamination with the virus is also an important mode of transmission.

Direct contact is important, as the virus will survive some hours in dried mucus particularly in cold and dry environments.

Diagnosis

Laboratory diagnosis depends upon the demonstration of the virus or its components or a rising antibody titre. The following tests are available:

· Direct antigen detection· RT-PCR for viral RNA · Virus culture(nasal pharyngeal aspirate preferably within 3 days of onset, other specimens, such as stool and rectal swabs may be considered.)

· Serological tests for detection of specific antibody. (blood test within 7 days of onset and repeated at least 2 weeks after onset.)

Incubation Period

The incubation period of a case will probably be one to four days.

Pathogenesis

Infection of pigs with influenza A viruses is of substantial importance to the swine industry and to the epidemiology of human influenza. At present, three main subtypes of influenza viruses are circulating in the swine population throughout the world: subtypes H1N1, H3N2, and H1N2. In North America, influenza virus outbreaks among pigs have historically been due almost exclusively to infection with H1N1 viruses. Since 1997-1998, however, H3N2 viruses have emerged and spread widely within the swine population. Triple-reassortant H3N2 viruses containing hemagglutinin (HA), neuraminidase (NA), and PB1 polymerase genes of human influenza virus origin, the matrix (M), nucleoprotein (NP), and nonstructural (NS) genes of classical swine influenza virus origin, and the PA and PB2 polymerase genes of avian influenza virus origin have been isolated widely throughout the United States. These viruses have been associated with outbreaks of respiratory disease in pigs of all ages and abortions in pregnant sows. In addition, reassortment between these viruses and classical H1N1 viruses has led to the subsequent development of H1N2 viruses, which have also spread throughout the swine population of the United States. In contrast, an H3N2 virus in which all eight RNA segments were of human influenza virus origin was isolated from a single baby pig in 1997 on a farm in Ontario, Canada. This virus did not spread within the farm of origin and has not been recovered from pigs subsequent to its initial isolation.

Influenza A viruses have been isolated from various species, including humans, pigs, horses, birds, sea mammals, and mink. However, wild waterfowl serve as the reservoir from which all influenza viruses are thought to have emerged. Despite their common origin, influenza A viruses are generally restricted in host range. In particular, avian influenza viruses replicate poorly in humans and nonhuman primates and human influenza viruses do not replicate well in birds. In contrast, swine influenza viruses have been shown repeatedly to infect humans as zoonotic infections, and conversely, human influenza viruses have also been isolated from pigs.

The host range restriction of influenza viruses is a polygenic trait, but the HA gene is considered to be a particularly important determinant since HA is responsible for attachment of the virus to sialic acid receptors on the host cell surface. While human influenza viruses preferentially bind to sialic acid bound to galactose by α2,6 linkages, avian viruses preferentially recognize sialic acid bound by α2,3 linkages. This is consistent with the fact that human tracheal epithelial cells predominantly express α2,6-linked receptors, whereas avian intestinal cells predominantly express α2,3-linked receptors. However, avian and human influenza viruses can both infect pigs because porcine respiratory epithelial cells express both N-acetylneuraminic acid-α2,3-galactose and N-acetylneuraminic acid-α2,6-galactose. Pigs can therefore function as intermediate “mixing vessel” hosts in establishing new influenza virus lineages by supporting coinfection, replication, and reassortment among human, avian, and swine influenza viruses.

Even though influenza viruses can cross species barriers and infect pigs, it is not known what properties are necessary to allow a virus to form a stable lineage and to spread efficiently within the pig population. In particular, a wholly human H3N2 virus, A/Swine/Ontario/00130/97 (H3N2) (Sw/ONT), initially crossed the species barrier to infect a pig in Canada in 1997, but it did not infect other pigs in the herd. Its disappearance may have been due to characteristics of the virus (i.e., its replication efficiency in pigs) or epidemiological factors (i.e., the availability of susceptible animals). In contrast, triple-reassortant H3N2 viruses containing genes from human, classical swine, and avian influenza viruses have spread throughout the swine population of the United States since 1998. The critical factors that affect replication ability in pigs may include the overall constellation of genes present in the triple-reassortant viruses. However, we have also identified specific differences in the sequences of the HA genes of triple-reassortant viruses that may represent swine adaptation mutations. As an initial step in understanding the pathogenesis of these viruses in pigs, the present study was designed to define the specific characteristics of these viruses, including their infectivities, replication kinetics, and ability to induce pathological lesions under experimental infection conditions.

Pathophysiology

Influenza virus infection occurs after transfer of respiratory secretions from an infected individual to a person who is immunologically susceptible. If not neutralized by secretory antibodies, the virus invades airway and respiratory tract cells. Once within host cells, cellular dysfunction and degeneration occur, along with viral replication and release of viral progeny. Systemic symptoms result from inflammatory mediators, similar to other viruses.

The most common complication of Influenza is Pneumonia. Other complications include Bronchitis, Sinus, Ear infections, Myocarditis, and Pericarditis. Myositis is among the complications but this one rarely occurs.